Microvascular Pathophysiology in Gastric Mucosal Inflammation Associated with Helicobacter pylori Infection

摘要

In the multitude of mechanisms involved in the development of gastric mucosal inflammation, derangement of the micro circulatory system is a common initial pathway. In response to gastric luminal antigens such as bacteria and food factors, the microvascular endothelium transduces signals to circulating cells. Helicobacter pylori colonization induces a significant level of leukocyte recruitment to the gastric mucosa as a result of the sequential pathological processes in the micro circulatory system. This bacterial infection is associated with a variety of clinical outcomes, including benign and malignant gastroduodenal diseases. After H. pylori inoculation, the bacteria colonize the surface epithelium, upon which numerous leukocytes rolling or adhering to the endothelial cells can be observed in the venules of the gastric mucosa. The adherent leukocytes migrate into the gastric mucosal parenchyma. Among the numerous proinflammatory factors, such as cytokines, free radicals, and enzymes, a monochloramine, derived from both leukocytes and H. pylori, is an important factor involved in the development of H. pylori-associated disease. Persistent H. pylori infection has recently been achieved in Mongolian gerbil models, in which the sequential micro circulatory and histopathological changes in the gastric mucosa have been shown to closely mimic the changes leading to gastric mucosal lesion formation in association with H. pylori infection in humans. Gastric mucosa infected with H. pylori exhibited significantly higher gastritis scores. Because the recently isolated growth-hormone-releasing peptide ghrelin is secreted mainly from the A-like cells in the gastric corpus, the anatomical extension of H. pylori-associated inflammation to the gastric corpus mucosa might also affect ghrelin secretion and its associated appetite control.